Abstract

Background

In healthy adolescents normal back shape asymmetry, here termed truncal asymmetry
(TA), is evaluated by higher and lower subsets of BMI. The study was initiated after
research on girls with adolescent idiopathic scoliosis (AIS) showed that higher and
lower BMI subsets discriminated patterns of skeletal maturation and asymmetry unexplained
by existing theories of pathogenesis leading to a new interpretation which has therapeutic
implications (double neuro-osseous theory).

Methods

5953 adolescents age 11–17 years (boys 2939, girls 3014) were examined in a school
screening program in two standard positions, standing forward bending (FB) and sitting
FB. The sitting FB position is thought to reveal intrinsic TA free from back humps
induced by any leg-length inequality. TA was measured in both positions using a Pruijs
scoliometer as angle of trunk inclinations (ATIs) across the back at each of three
spinal regions, thoracic, thoracolumbar and lumbar. Abnormality of ATIs was defined
as being outside 2 standard deviations for each age group, gender, position and spinal
region, and termed severe TA.

Results

In the sitting FB position after correcting for age,relatively lower BMIs are statistically associated with a greater number of severe TAs than with relatively
higher BMIs in both girls (thoracolumbar region) and boys (thoracolumbar and lumbar
regions).

The relative frequency of severe TAs is significantly higher in girls than boys for
each of the right thoracic (56.76%) and thoracolumbar (58.82%) regions (p = 0.006,
0.006, respectively). After correcting for age, smaller BMIs are associated with more
severe TAs in boys and girls.

Discussion

BMI is a surrogate measure for body fat and circulating leptin levels. The finding
that girls with relatively lower BMI have significantly later menarche, and a significant
excess of TAs, suggests a relation to energy homeostasis through the hypothalamus.
The hypothesis we suggest for the pathogenesis of severe TA in girls and boys has
the same mechanism as that proposed recently for AIS girls, namely: severe TAs are
initiated by a genetically-determined selectively increased hypothalamic sensitivity (up-regulation, i.e. increased sensitivity) to
leptin with asymmetry as an adverse response to stress (hormesis), mediated bilaterally
mainly to the growing trunk via the sympathetic nervous system (leptin-hypothalamic-sympathetic nervous system (LHS) concept). The putative autonomic dysfunction is thought to be increased by any lower circulating
leptin levels associated with relatively lower BMIs. Sympathetic nervous system activation
with asymmetry leads to asymmetries in ribs and/or vertebrae producing severe TA when
beyond the capacity of postural mechanisms of the somatic nervous system to control
the shape distortion of the trunk. A test of this hypothesis testing skin sympathetic
responses, as in the Rett syndrome, is suggested.